The human heart is a pump comprising four chambers. The two smaller chambers, the left and right atria, are in the upper part of the heart and the two larger chambers, the left and right ventricles, are in the lower part. The heart pumps by the contractions of the strong muscles which make up the outer walls of the four chambers. During normal operation blood returning from the body is collected in the right atrium. When the right atrium becomes substantially full of blood, it contracts forcing blood through the tricuspid valve into the right ventricle. Contractions of the right ventricle send blood in pulses through the large pulmonary artery and into each lung where the blood becomes oxygenated before it returns through the pulmonary veins to fill the left atrium of the heart. Upon filling with blood, the left atrium contracts, squeezing blood through the mitral valve to the left ventricle. In the final step of the operational cycle of the heart, the powerful muscles of the left ventricle contract forcing oxygen-rich blood through the aorta, then into the smaller arteries to eventually deliver blood to tissue throughout the body. The left and right atria and left and right ventricles contract together, so that the heart functions essentially like two ganged two stage pumps.
Improper operation of the valves or failure of the valves to seal properly can significantly affect the efficiency of most pumps and the heart is no exception. Failure of the valves of the heart to function properly can lead to serious health problems or death. Fortunately, medical science has developed techniques to correct certain heart valve problems in some patients, but finding appropriate remedies for heart valve imperfections and failures while minimizing trauma to the patient is still a major challenge for cardiologists and cardiac surgeons.
Each atrioventricular valve is comprised of a number of cusps, many chordae tendineae which act as guy wires or like shrouds of a parachute to stabilize and keep the cusps in postion when closed, and papillary muscles to which the chordae are anchored. If the chordae tendineae are weak or stretched, the cusps which they stabilize may not seal when closed or may even pop backward into the atrium when the ventricle contracts, a condition known as prolapse.
The chordae tendineae may be divided into three groups or "orders". The first group extending from near the apices of the papillary muscles to near the edges of the valve which they stabilize. The tendinous cords subdivide into thinner strands as they near the valve edge. The chordae of the first order insert into the extreme edge of the valve by a large number of very fine strands. Their function seems to be merely to prevent eversion of the opposing borders of the cusps.
The chordae of the second order insert on the ventricular surface of the cusps approximately at the level of the noduli Albini or even higher. These are stronger and less numerous that those of the first order. These function as the mainstays of the valve and are comparable to the stays of an umbrella.
The chordae of the third order originate from the ventricular wall much nearer the origin of the cusps and often form bands or foldlike structures which may contain muscle. Occasionally, particularly on the left side, the chordae of the first two orders, even in normal hearts, may be wholly muscular, so that the papillary muscle seems to insert directly into the cusp. This is not surprising because the papillary muscle, the chordae tendineae, and major parts of the cusps are derived from the embryonic ventricular myocardium and therefore, were all muscular at one time (see Van Mierop, L. H. S. "Anatomy of the Heart," page 67, Clinical Symposia, Ciba-Geigy, Summit, N.J. (1965)).
Collagen-containing connective tissue is ubiquitous in the human body and demonstrates several unique characteristics not found in other tissue. It provides the cohesiveness of the musculoskeletal system, the structural integrity of the viscera as well as the elasticity of integument. Intermolecular cross links provide collagen connective tissue with unique physical properties of high tensile strength and substantial elasticity. Collagen fibers shrink and tighten when elevated in temperature. This unique molecular response to temperature elevation is the result of rupture of the collagen stabilizing cross links and immediate contraction of the collagen fibers to about one-third of their original linear dimension. Additionally, the caliber of the individual fibers increases greatly, over four fold, without changing the structural integrity of the connective tissue.
One technique for altering collagen connective tissue involves heating the tissue by means of infrared laser energy. Another technique involves inducing heat in the tissue by exposure to radio frequency (rf) or microwave radiation. It is also possible to heat the collagen tissue directly by contact with a warm probe or catheter heated with electricity or by circulation of a heated fluid. The use of infrared laser energy as a corneal collagen shrinking tool of the eye has been described and relates to laser keratoplasty (see U.S. Pat. No. 4,976,709). The importance of controlling the delivery of the energy, that is controlling the localization, time, and intensity, of the energy is critical to provide the soft tissue shrinkage effects without excess collateral damage. Another technique for altering collagen is taught in U.S. Pat. No. 5,458,596 to treat joints.
There is a need to remodel, e.g., strengthen, tighten, and shorten, tissue of the heart to correct faults and increase cardiac efficiency in certain patients. In particular, the chordae tendineae can be tightened to prevent valve prolapse. The art teaches that such remodeling in some cases can be achieved by surgical manipulation, usually requiring open heart surgery, a major, complicated operation. A less invasive remodeling procedure is needed which would lower the risk to the patient.
Copending U.S. patent application Ser. No. 08/739,820, filed Oct. 30, 1996, now U.S. Pat. No. 5,827,268 teaches heating heart tissue with a heat producing catheter as a treatment for Patent Ductus Arteriosus. Further, copending U.S. patent application Ser. No. 08/768,607, filed Dec. 18, 1996 discloses a device and treatment by heating collagen tissue of the heart to repair damage from a myocardial infarction.
It is an object of the present invention to provide a technique for improving atrioventricular valve performance and preventing prolapse by remodeling the corresponding chordae tendineae with heat. It is also an object to provide devices for this remodeling technique as well as methods of teaching the technique.